Gout
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Gout: What It Is, Symptoms & Causes UK
A clinically reviewed conditions guide to gout — what it is, how attacks happen, common sites, risk factors, diagnosis, and an overview of acute and preventive treatment.
Gout is the most common form of inflammatory arthritis in the UK, affecting around 2.5% of the adult population. It is caused by the deposition of monosodium urate crystals in joints, producing sudden, intensely painful attacks. It is highly treatable — both the acute attack and long-term prevention. Most people can achieve complete control with the right management.
What Is Gout?
Gout is a form of crystal arthropathy — distinct from degenerative conditions like osteoarthritis — a type of arthritis caused by the deposition of crystals within a joint. In gout, the crystals are monosodium urate, which form when uric acid levels in the blood become chronically elevated (hyperuricaemia). When uric acid exceeds its solubility threshold in the synovial fluid of a joint, it crystallises out of solution and deposits in and around the joint.
The crystals themselves are not the immediate cause of pain — the immune system’s response to them is. The body recognises monosodium urate crystals as foreign material and mounts a powerful inflammatory reaction, flooding the joint with inflammatory mediators including interleukin-1β (IL-1β), prostaglandins, and neutrophils. It is this inflammatory cascade that produces the intense heat, swelling, redness, and pain of a gout attack.
How a Gout Attack Happens
Gout attacks typically begin suddenly, often overnight, and progress rapidly to maximum intensity within 12–24 hours. The sequence:
- Trigger — a sudden change in uric acid levels (a rich meal, alcohol, dehydration, starting a diuretic, surgery, or an acute illness) can precipitate crystal shedding from existing joint deposits
- Crystal shedding — crystals shed from existing deposits into the synovial fluid, or new crystals form during supersaturation
- Immune activation — macrophages in the joint recognise the crystals and release IL-1β; this cascades into a massive local inflammatory response
- Peak attack — the joint becomes acutely hot, swollen, red, and exquisitely tender; even the weight of a bedsheet can be intolerable
- Resolution — the inflammatory response gradually subsides over 7–10 days untreated; with NSAIDs, typically 3–5 days
Symptoms of a Gout Attack
- Sudden onset severe joint pain — characteristically described as one of the worst pain experiences; often wakes patients from sleep
- Swelling and inflammation — the affected joint is visibly swollen, often dramatically so
- Redness and warmth — the overlying skin becomes hot and red; can resemble cellulitis (skin infection)
- Extreme tenderness — even light touch or the weight of a sheet is painful; the joint is usually not bearable to examine properly during an acute attack
- Limited movement — the joint cannot be moved through its full range due to pain and swelling
- Prodrome — some patients experience mild discomfort or joint warmth hours before the full attack begins
Between attacks, gout joints may appear and feel completely normal. This intercritical phase can last months or years but does not mean gout has resolved — uric acid crystals remain deposited and serum urate is still elevated.
Common Sites Affected
| Joint | Frequency | Notes |
|---|---|---|
| First metatarsophalangeal (big toe) | ~70% of first attacks | Classic presentation — podagra; peripheral location favours crystal deposition (lower temperature) |
| Ankle | Common | Often presents as acute ankle swelling; can mimic sprain |
| Knee | Common | Large joint; effusion often visible |
| Wrist and midfoot | Less common | More common in women and with longer disease duration |
| Polyarticular gout | More common in chronic gout | Multiple joints involved simultaneously; more common with severe hyperuricaemia and in women |
Causes and Risk Factors
Gout is ultimately caused by hyperuricaemia — chronically elevated serum uric acid. Uric acid is the end product of purine metabolism. Purines are broken down via xanthine oxidase to uric acid, which is filtered by the kidneys. Gout develops when either uric acid production is excessive, renal excretion is impaired, or both.
| Risk factor category | Examples |
|---|---|
| Diet | Red meat, organ meats (high purine); shellfish; beer and spirits; fructose-containing drinks |
| Alcohol | Beer and spirits more strongly implicated than wine; alcohol both increases uric acid production and reduces renal excretion |
| Medications | Thiazide and loop diuretics (most common drug cause); low-dose aspirin; ciclosporin; pyrazinamide |
| Medical conditions | Chronic kidney disease (reduced uric acid excretion); hypertension; metabolic syndrome; heart failure; psoriasis |
| Genetics | Strong familial tendency; variants in uric acid transporter genes (SLC2A9, ABCG2) are well-established risk loci |
| Sex and age | Men 4× more commonly affected; women’s risk rises after menopause as oestrogen’s uricosuric effect is lost |
| Dehydration | Reduces renal urate clearance; common trigger for acute attacks |
Stages of Gout
- Asymptomatic hyperuricaemia — elevated serum urate without clinical gout; most people with raised urate never develop gout
- Acute gout — the first or subsequent attacks; complete resolution between attacks
- Intercritical gout — the asymptomatic period between attacks; duration varies from weeks to years; crystals remain present
- Chronic tophaceous gout — without urate-lowering treatment, tophi (chalk-like urate crystal deposits) develop under the skin and in soft tissues; joint damage accumulates
How Gout Is Diagnosed
Definitive diagnosis requires identification of monosodium urate crystals in synovial fluid (needle-shaped, negatively birefringent on polarised light microscopy). In practice, most gout is diagnosed clinically — based on the characteristic presentation, affected joint, and elevated serum urate — without joint aspiration.
Serum urate can be falsely normal or low during an acute attack (the inflammatory response alters urate distribution), so should be checked 4–6 weeks after the attack resolves. Renal function, FBC, and lipids are typically checked at diagnosis. X-ray findings are often normal in early gout; erosions and joint damage appear in chronic disease.
Treatment Overview
Treatment addresses two distinct goals: ending the acute attack, and preventing future attacks by lowering serum urate long-term.
| Goal | Approach |
|---|---|
| Acute attack | NSAIDs (naproxen is NICE first-line), colchicine, or short-course corticosteroids. Start treatment as soon as the attack begins for best effect. Rest and elevate the joint. Ice packs may help. |
| Prevention | Urate-lowering therapy (allopurinol first-line; febuxostat if allopurinol not tolerated). Target serum urate <360 µmol/L (or <300 µmol/L in tophaceous gout). Lifestyle modification: reduce alcohol, high-purine foods, and fructose; stay hydrated; review diuretic use where possible. |
For prescription gout treatment — naproxen, colchicine, and urate-lowering therapy: Gout treatment at Access Doctor →
When to Seek Help
Seek medical advice for a confirmed or suspected first gout attack — a clinical assessment is needed to confirm the diagnosis and start treatment. See a GP also if:
- Attacks are becoming more frequent or involving more joints
- You are developing visible tophi under the skin
- Your current treatment is not controlling attacks adequately
- You have concerns about urate-lowering medication
Seek urgent care if an inflamed joint is accompanied by high fever and rigors — this may indicate septic arthritis (infected joint), which requires emergency assessment and is distinct from gout despite similar presentation.
Frequently Asked Questions
What causes gout?
Gout is caused by elevated uric acid in the blood (hyperuricaemia). When uric acid exceeds its solubility threshold, monosodium urate crystals deposit in joints. Risk factors include diet (red meat, alcohol, shellfish), diuretic medications, chronic kidney disease, metabolic syndrome, and genetics. Men are four times more commonly affected than women.
What does a gout attack feel like?
A gout attack typically begins suddenly, often overnight, reaching peak intensity within 12–24 hours. The affected joint — most commonly the big toe — becomes severely painful, visibly swollen, hot, and red. Even the weight of a bedsheet on the joint is often intolerable. Untreated attacks resolve over 7–10 days.
How is gout treated?
Acute attacks are treated with NSAIDs (naproxen is NICE first-line), colchicine, or short-course corticosteroids, started as early as possible. Long-term prevention uses urate-lowering therapy — allopurinol is first-line — targeting serum urate below 360 µmol/L.
Can I get prescription gout treatment online?
Yes. Access Doctor prescribes NSAIDs (including naproxen) for acute gout following an online clinical consultation. GPhC-registered pharmacist independent prescribers. GPhC pharmacy #9011198.
What foods should I avoid with gout?
The main dietary triggers are organ meats (liver, kidney), red meat, shellfish (especially mussels, scallops, anchovies), beer and spirits, and fructose-containing drinks. Staying well hydrated is also important. Dietary changes alone rarely normalise uric acid sufficiently — medication is usually needed for recurrent gout.
References
- NICE CKS. Gout. Updated 2023. cks.nice.org.uk/topics/gout
- BNF. Gout. bnf.nice.org.uk
- Dalbeth N et al. Gout. Lancet. 2021.
- NHS. Gout. nhs.uk/conditions/gout
Medical disclaimer: This article is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional. In a medical emergency, call 999.
